Loss of Expression of the p16/Cyclin-dependent Kinase Inhibitor 2 Tumor Suppressor Gene in Melanocytic Lesions Correlates with Invasive Stage of Tumor Progression

摘要: Abstract Sporadic and familial malignant melanoma susceptibility has been linked to defects in the chromosomal region 9p21. Recently, a putative 9p21 tumor suppressor gene, cyclin dependent kinase inhibitor 2 ( CDKN2 ) or p16 shown be deleted, mutated, rear-ranged high percentage of sporadic cell lines, as well mutated germline proportion patients. encodes M r 16,000 protein (p16) that plays key role cycle control by binding cyclin-dependent 4 enzyme inhibiting its ability phosphorylate critical substrates necessary for transition past G 1 phase cycle. Thus, mutations deletions gene could result abnormal proliferation via defective control. The correlation cytogenetic molecular alterations with clinical stages progression suggests dysfunction within this is evolution melanoma. However, it remains unclear whether gene. If so, then loss potentially an initiating early event progression. To address issues what potential involvement precisely when during clinically evident occur, we have evaluated immunohistochemistry expression 103 melanocytic lesions representing all Our results suggest not initiation because melanomas situ majority primary invasive retain protein; b more related invasiveness metastasize, 52% tumors 72% metastatic show partial complete p16.